ArticleNature communications2011
Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance.
Article in Nature communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 124 citations in OpenAlex.
- Expert consensus on diagnostic guidelines for pediatric inflammatory bowel disease in Japan.Journal of gastroenterology · 2025Review
- UDCA ameliorates inflammation driven EMT by inducing TGR5 dependent SOCS1 expression in mouse macrophages.Scientific reports · 2024Article
- Suppressor of Cytokine Signaling Proteins 3 and 5 Potentially Delineate Polarization of Th cells in Chronic Rhinosinusitis.The Yale journal of biology and medicine · 2024Article
- A new type of sulfation reaction:PNAS nexus · 2024Article
- Prostaglandin ENature communications · 2024Article
- The Promotion of Humoral Immune Responses in Humans via SOCS1-Mediated Th2-Bias Following SARS-CoV-2 Vaccination.Vaccines · 2023Article
- KIAA0317 regulates SOCS1 stability to ameliorate colonic inflammation.The FEBS journal · 2023Article
- Distinct transcriptional signatures in purified circulating immune cells drive heterogeneity in disease location in IBD.BMJ open gastroenterology · 2023Article
- Review
- Effects of human induced pluripotent stem cell-derived intestinal organoids on colitis-model mice.Regenerative therapy · 2022Article
- Maternal stevioside supplementation improves intestinal immune function of chicken offspring potentially via modulating gut microbiota and down-regulating the promoter methylation level of suppressor of cytokine signaling 1 (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2022Article
- Characterization of Maladaptive Processes in Acute, Chronic and Remission Phases of Experimental Colitis in C57BL/6 Mice.Biomedicines · 2022Article
- Prostaglandin E-major urinary metabolite diagnoses mucosal healing in patients with ulcerative colitis in remission phase.Journal of gastroenterology and hepatology · 2022Article
- Facilitation of colonic T cell immune responses is associated with an exacerbation of dextran sodium sulfate-induced colitis in mice lacking microsomal prostaglandin E synthase-1.Inflammation and regeneration · 2022Article
- Colonic healing requires Wnt produced by epithelium as well as Tagln+ and Acta2+ stromal cells.Development (Cambridge, England) · 2022Article
- Hyaluronic Acid Increases Anti-Inflammatory Efficacy of Rectal 5-Amino Salicylic Acid Administration in a Murine Colitis Model.Biomolecules & therapeutics · 2021Article
- Human Oral Epithelial Cells Suppress T Cell FunctionFrontiers in immunology · 2021Article
- SOD1 suppresses pro-inflammatory immune responses by protecting against oxidative stress in colitis.Redox biology · 2020Article
- Intestinal Macrophages at the Crossroad between Diet, Inflammation, and Cancer.International journal of molecular sciences · 2020Review
- The chemopreventive effect of 5-demethylnobiletin, a unique citrus flavonoid, on colitis-driven colorectal carcinogenesis in mice is associated with its colonic metabolites.Food & function · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin 10 (IL-10) and regulatory T cells (Tregs) maintain tolerance to intestinal microorganisms. However, Il10(-/-)Rag2(-/-) mice, which lack IL-10 and Tregs, remain healthy, suggesting the existence of other mechanisms of tolerance. Here, we identify suppressor of cytokine signalling 1 (SOCS1) as an essential mediator of immune tolerance in the intestine. Socs1(-/-)Rag2(-/-) mice develop severe colitis, which can be prevented by the reduction of microbiota and the transfer of IL-10-sufficient Tregs. Additionally, we find an essential role for prostaglandin E2 (PGE2) in the maintenance of tolerance within the intestine in the absence of Tregs. Socs1(-/-) dendritic cells are resistant to PGE2-mediated immunosuppression because of dysregulated cytokine signalling. Thus, we propose that SOCS1 and PGE2, potentially interacting together, act as an alternative intestinal tolerance mechanism distinct from IL-10 and Tregs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.